30.4.18

Sweaty workout dampens appetite

Exercise suppresses eating by heating up a region of the brain called the hypothalamus, according to a study in mice.
Although it has long been clear that exercise can reduce appetite,
the mechanism behind this effect has not been clear.
Young-Hwan Jo and
his colleagues at the Albert Einstein College of Medicine in New York
City found that a class of brain cells in the hypothalamus that affect
appetite also bear proteins called TRPV1-like receptors. These receptors
respond to changes in temperature.
The team found that, in mice, a stint on the treadmill both raised
the temperature of the hypothalamus and reduced eating. The same dual
effect was seen after artificial stimulation of the neurons that express
TRPV1-like receptors. Conversely, when the researchers turned down
expression of the neurons’ Trpv1 gene, mice did not curb their food
intake after exercise.

The study was published in the journal PLoS Biology.
Also, children are more physically fit, by some measures, than nationally competitive runners and cyclists.
Parents have long noted that children do not tire as quickly as
adults — an observation that has been confirmed by scientists. To
compare the two groups, Sébastien Ratel at the University of Clermont
Auvergne in Clermont-Ferrand, France, and his colleagues tested the
fitness of two groups of adults — university students and elite
endurance athletes — and compared them with eight–12-year-old boys who
did not regularly engage in strenuous physical training.
After intense workouts on a stationary bike, the boys’ heart rates
returned to normal faster than those of both groups of adults. The
children also eliminated lactate — a metabolic by-product that
contributes to muscle fatigue — from their blood faster than the adults
did.
Although the number of children enrolled in the study was small, the
researchers say their results show that children’s muscle endurance is
naturally high but falls on the path to adulthood.
The study was published in Frontier of Physiology.
Also, doctors, health organizations, and the Surgeon General all
agree that exercise is good for the heart — but the reasons why are
still not well understood.
In a new study performed in mice, researchers from the Harvard
Department of Stem Cell and Regenerative Biology (HSCRB), Massachusetts
General Hospital (MGH) and Harvard Medical School (HMS), and the Harvard
Stem Cell Institute (HSCI), United States, uncovered one reason why
exercise might be beneficial: it stimulates the heart to make new muscle
cells, both under normal conditions and after a heart attack.
Published in Nature Communications on 25 April, the findings have
implications for public health, physical education and the
rehabilitation of cardiac patients.
The human heart has a relatively low capacity to regenerate itself.
Young adults can renew around one per cent of their heart muscle cells
every year, and that rate decreases with age. Considering that losing
heart cells is linked to heart failure, interventions that increase new
heart cell formation have potential to prevent heart failure.
The two first authors on the study were Ana Vujic, Ph.D. of HSCRB, and Carolin Lerchenmüller, M.D. of MGH and HMS.
“We wanted to know whether there is a natural way to enhance the
regenerative capacity of heart muscle cells,” said Vujic. “So we decided
to test the one intervention we already know to be safe and
inexpensive: exercise.”
To test the effects of exercise, the researchers gave one group of
healthy mice voluntary access to a treadmill. When left to their own
devices, the mice ran around five kilometers each day. The other healthy
group had no such gym membership, and remained sedentary.
To measure heart regeneration in the mice, the researchers
administered a labelled chemical that was incorporated into newly made
DNA as cells prepared to divide. By following the labelled DNA in the
heart muscle, they could see where new cells were being produced.
The researchers found that the exercising mice made over four and a
half times the number of new heart muscle cells than the mice without
treadmill access.
The results were certainly significant — but were they relevant? To
find out, the researchers brought the experiment a little closer to
home.
“We also wanted to test this in the disease setting of a heart attack, because our main interest is healing,” said Vujic.
After experiencing a heart attack, mice with treadmill access still
ran five kilometers a day, voluntarily. Compared to their sedentary
counterparts, the exercising mice showed an increase in the area of
heart tissue where new muscle cells were made.
The conclusion: in mice, exercise means regenerating heart tissue — a lot.
The two senior authors behind the study were Richard Lee, M.D.,
Harvard Professor of Stem Cell and Regenerative Biology, and Principal
Faculty member of HSCI, and Anthony Rosenzweig, M.D., Paul Dudley White
Professor of Medicine at HMS, Chief of the Cardiology Division at MGH,
and Principal Faculty member of HSCI.
“Maintaining a healthy heart requires balancing the loss of heart
muscle cells due to injury or aging with the regeneration or birth of
new heart muscle cells. Our study suggests exercise can help tip the
balance in favor of regeneration,” said Rosenzweig.
“Our study shows that you might be able to make your heart younger by exercising more every day,” said Lee.
It’s all very well to say that exercise is good for the heart — but
how does that actually work? To find out, the researchers plan to
pinpoint which biological mechanisms link exercise with increased
regenerative activity in the heart.
In this study, the researchers identified a specific biological
pathway that is required for exercise to turn on cardiac regeneration.
“Now we need to find the signals that are sufficient to turn this
pathway on,” said Rosenzweig.
“If we can turn on these pathways at just the right time, in the
right people, then we can improve recovery after a heart attack,” said
Lee.